Editing Liposarcoma

{{Short description|Tumor originating in adipose (fat) tissue}}
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{{Infobox medical condition (new)
| name            = Liposarcoma
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| image           = Histopathology of liposarcoma, annotated.jpg
| caption         = Histopathology of liposarcoma, H&E stain:<ref name=PathologyOutlines>{{cite web|url=https://www.pathologyoutlines.com/topic/softtissuewdliposarcoma.html | vauthors = Potterveld S, Clay MR  |website=PathologyOutlines|title=Liposarcoma}} Topic Completed: November 2017. Minor changes: May 2023</ref><br />-
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| field           = [[Dermatology]], [[general surgery]] [[oncology]]
| symptoms        = Lump under skin, pain, swelling, organ dysfunction
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'''Liposarcomas''' are the most common subtype of soft tissue [[sarcoma]]s, accounting for at least 20% of all sarcomas in adults.<ref name="pmid33355009">{{cite journal | vauthors = Nie L, Chen X, Gong J, Zhang M, Xu M, Chen N, Zhou Q | title = Synchronous Renal Dedifferentiated Liposarcoma and Retroperitoneal Well-Differentiated Liposarcoma: A Case Report With Literature Review | journal = International Journal of Surgical Pathology | volume = 29| issue = 6| pages = 667–671 | date = December 2020 | pmid = 33355009 | doi = 10.1177/1066896920981682 | s2cid = 229688954 | url = }}</ref> Soft tissue sarcomas are rare [[neoplasms]] with over 150 different [[histological]] subtypes or forms. Liposarcomas arise from the precursor [[lipoblast]]s of the [[adipocytes]] (i.e. fat cells) in [[adipose tissue|adipose (i.e. fat) tissues]]. Adipose tissues are distributed throughout the body, including such sites as the deep and more superficial layers of [[subcutaneous tissue]]s as well as in less surgically accessible sites like the [[Retroperitoneal space|retroperitoneum]] (i.e. space behind the [[abdominal cavity]]) and [[Adipose tissue#Visceral fat|visceral fat]] inside the [[abdominal cavity]].<ref name="pmid10982304">{{cite journal | vauthors = Dei Tos AP | title = Liposarcoma: new entities and evolving concepts | journal = Annals of Diagnostic Pathology | volume = 4 | issue = 4 | pages = 252–266 | date = August 2000 | pmid = 10982304 | doi = 10.1053/adpa.2000.8133 }}</ref>

All liposarcomas consist of at least some cells that bear a resemblance to fat cells when examined for their [[histopathologic]] appearances under a microscope.<ref>{{Cite web|url = http://sarcomahelp.org/liposarcoma.html|title = What is Liposarcoma?|date = October 2012|access-date = 2015-04-22|website = The Liddy Shriver Sarcoma Initiative| vauthors = Bell T }}</ref> However, the liposarcomas do have several forms based on differences in their [[Physical examination|clinical presentations]] (e.g. ages, gender preferences, sites of tumors, [[signs and symptoms|signs]], and [[signs and symptoms|symptoms]]), severities (i.e. potential to [[Invasion (cancer)|invade]] local tissues, recur after surgical removal, and [[metastasize]] to distal tissues), [[Genetic disorder|genetic abnormalities]], prognoses, and preferred treatment regimens. The [[World Health Organization]] in 2020 reclassified liposarcomas into five more or less distinct forms: '''1)''' atypical lipomatous tumor/well-differentiated liposarcoma (WD-LPS); '''2)''' dedifferentiated liposarcoma (DD-LPS); '''3)''' myxoid liposarcoma; '''4)''' pleomorphic liposarcoma; and '''5)''' myxoid pleomorphic liposarcoma.<ref name="pmid34191084">{{cite journal | vauthors = Porrino J, Al-Dasuqi K, Irshaid L, Wang A, Kani K, Haims A, Maloney E | title = Update of pediatric soft tissue tumors with review of conventional MRI appearance-part 1: tumor-like lesions, adipocytic tumors, fibroblastic and myofibroblastic tumors, and perivascular tumors | journal = Skeletal Radiology | volume = 51| issue = 3| pages = 477–504| date = June 2021 | pmid = 34191084 | doi = 10.1007/s00256-021-03836-2 | s2cid = 235678096 | url = }}</ref> ([[Pleomorphism (cytology)|Pleomorphic]] indicates the presence of cells that have abnormal and often large variations in their size and shape and/or the size and shape of their nuclei.)

While liposarcoma forms are classified as being aggressive and [[malignant]] or, in the case of the atypical lipomatous tumor/well-differentiated liposarcoma, as relatively non-aggressive and benign,<ref name="pmid33659920">{{cite journal | vauthors = Haddox CL, Riedel RF | title = Recent advances in the understanding and management of liposarcoma | journal = Faculty Reviews | volume = 10 | issue = | pages = 1 | date = 2021 | pmid = 33659920 | pmc = 7894267 | doi = 10.12703/r/10-1 | url =  | doi-access = free }}</ref> all five liposarcoma forms can infiltrate locally to injure nearby tissues and organs, occur in surgically inaccessible sites adjacent to vital organs (e.g. the retroperitoneum<ref name="pmid21274402">{{cite journal | vauthors = Nishio J | title = Contributions of cytogenetics and molecular cytogenetics to the diagnosis of adipocytic tumors | journal = Journal of Biomedicine & Biotechnology | volume = 2011 | issue = | pages = 524067 | date = 2011 | pmid = 21274402 | pmc = 3025394 | doi = 10.1155/2011/524067 | url = | doi-access = free }}</ref>), recur after surgical removal, and progress to life-threatening diseases. Studies to date find that all five liposarcoma forms, while usually treatable at least initially by surgical resection, are often only marginally responsive to currently used [[chemotherapy]] and [[radiotherapy]] regimens. The liposarcomas require a wide range of further studies to determine their responsiveness to various [[radiotherapy]], [[chemotherapy]], and more novel treatment regimens as used individually and in various combinations that would include, where possible, surgical removal.<ref name="pmid33659920"/>

==Etymology==
"fatty tumor" (plural lipomata), 1830, medical Latin, from Greek lipos "fat" (n.), from PIE root *leip- "to stick, adhere", also used to form words for "fat", + -oma.

1650s, "fleshy excrescence", (plural liposarcomata), Medical Latin, from Latinized form of Greek sarkoma "fleshy substance" (Galen), from sarkoun "to produce flesh, grow fleshy", from sarx (genitive sarkos) "flesh", + -oma.

==Forms of liposarcomas==
[[File:Lipoblast features, annotated.png|thumb|Lipoblast features.]]
Liposarcomas are generally large tumors (>10&nbsp;cm) but can be of almost any size. They occur mainly in adults with only 0.7% of cases occurring in those <16 years old.<ref name="pmid34191084"/> In adults,  liposarcomas occur predominantly in and after middle-age.<ref name="pmid30852045">{{cite journal | vauthors = Thway K | title = Well-differentiated liposarcoma and dedifferentiated liposarcoma: An updated review | journal = Seminars in Diagnostic Pathology | volume = 36 | issue = 2 | pages = 112–121 | date = March 2019 | pmid = 30852045 | doi = 10.1053/j.semdp.2019.02.006 | s2cid = 73725589 | url = }}</ref> The very rare cases occurring in children and adolescents are diagnosed predominantly as being the myxoid liposarcoma form.<ref name="pmid34191084"/>

The five liposarcoma forms must be distinguished not only from each other but also from certain other soft tissue tumors. These other tumors along with some of their distinguishing histopathologic features are: '''1)''' dysplastic lipomas (i.e. benign humors that have sites of tissue [[necrosis]] and neoplastic, variably-sized fat cells containing variable sized/shaped [[Cell nucleus|nuclei]]; these neoplastic cells, unlike most neoplastic cell in the liposarcomas, do not [[Gene expression|overexpress]] the ''[[MDM2]]'' gene);<ref name="pmid30001242">{{cite journal | vauthors = Michal M, Agaimy A, Contreras AL, Svajdler M, Kazakov DV, Steiner P, Grossmann P, Martinek P, Hadravsky L, Michalova K, Svajdler P, Szep Z, Michal M, Fetsch JF | title = Dysplastic Lipoma: A Distinctive Atypical Lipomatous Neoplasm With Anisocytosis, Focal Nuclear Atypia, p53 Overexpression, and a Lack of MDM2 Gene Amplification by FISH; A Report of 66 Cases Demonstrating Occasional Multifocality and a Rare Association With Retinoblastoma | journal = The American Journal of Surgical Pathology | volume = 42 | issue = 11 | pages = 1530–1540 | date = November 2018 | pmid = 30001242 | doi = 10.1097/PAS.0000000000001129 | s2cid = 51616357 | url = }}</ref> '''2)''' atypical [[spindle cell lipoma]]s (i.e. benign tumors with mildly atypical spindle-shaped cells in a fibrous-to-myxoid [[stroma (tissue)|stroma]] intermixed with vacuolated [[lipoblast]]s and variable-sized adipocytes with atypical nuclei; '''3)''' [[pleomorphic lipoma]]s (i.e. benign tumors characterized by giant cells with overlapping nuclei);<ref name="pmid30852045"/> and '''4)''' [[solitary fibrous tumor]]s (i.e. tumors, up to 22% of which exhibit malignant behavior, consisting of spindle- or ovoid-shape cells within a collagenous background stroma  intermixed with blood vessels with a characteristic staghorn shape<ref name="pmid34200924">{{cite journal | vauthors = Martin-Broto J, Mondaza-Hernandez JL, Moura DS, Hindi N | title = A Comprehensive Review on Solitary Fibrous Tumor: New Insights for New Horizons | journal = Cancers | volume = 13 | issue = 12 | date = June 2021 | page = 2913 | pmid = 34200924 | pmc = 8230482 | doi = 10.3390/cancers13122913 | url = | doi-access = free }}</ref>).<ref name="pmid34191084"/>

===Atypical lipomatous tumor/well-differentiated liposarcoma===
Together, atypical lipomatous tumors (ALTs) and well-differentiated liposarcomas (WDLs) account for 40{{ndash}}45% of all liposarcomas.<ref name="pmid18000364">{{cite journal | vauthors = Hameed M | title = Pathology and genetics of adipocytic tumors | journal = Cytogenetic and Genome Research | volume = 118 | issue = 2–4 | pages = 138–47 | date = 2007 | pmid = 18000364 | doi = 10.1159/000108294 | s2cid = 27183708 | url = }}</ref> They rarely if ever [[metastasize]] and therefore are regarded as [[Benign tumor|benign]] or [[Precancerous condition|premalignant]] tumors.<ref name="pmid33734108"/><ref name="pmid30397612">{{cite journal | vauthors = Usuda D, Takeshima K, Sangen R, Nakamura K, Hayashi K, Okamura H, Kawai Y, Kasamaki Y, Iinuma Y, Saito H, Kanda T, Urashima S | title = Atypical lipomatous tumor in the ligamentum teres of liver: A case report and review of the literature | journal = World Journal of Clinical Cases | volume = 6 | issue = 12 | pages = 548–553 | date = October 2018 | pmid = 30397612 | pmc = 6212614 | doi = 10.12998/wjcc.v6.i12.548 | url =  | doi-access = free }}</ref> However, they are locally invasive and may [[Malignant transformation|transform]] to a more aggressive and potentially metastasizing liposarcoma, i.e. a dedifferentiated liposarcoma. Furthermore, a surgically removed atypical lipomatous tumor/well-differentiated liposarcoma may recur as a dedifferentiated liposarcoma.<ref name="pmid33659920"/>

====Presentation====
[[Image:edemaliposarcoma.jpg|thumb|right|Left leg swelling caused by underlying liposarcoma]]
ALTs and WDLs are considered virtually identical tumors except that by definition ALTs designate tumors that develop in the arms or legs while WDLs designate tumors that develop in less surgically accessible sites such as the deep, centrally-located soft tissues of the [[retroperitoneum]], paratesticular region (i.e. area within the [[scrotum]] including the [[testes]], [[spermatic cord]], [[Tunica albuginea of testis|testicular tunic]], [[epididymis]], and [[appendix of testis]]),<ref name="pmid33659920"/> [[oral cavity]], and [[eye socket]].<ref name="pmid33734108">{{cite journal | vauthors = Pei J, Flieder DB, Talarchek JN, Cooper HS, Patchefsky AS, Wei S | title = Clinical Application of Chromosome Microarray Analysis in the Diagnosis of Lipomatous Tumors | journal = Applied Immunohistochemistry & Molecular Morphology | volume = 29| issue = 8| pages = 592–598| date = March 2021 | pmid = 33734108 | doi = 10.1097/PAI.0000000000000923 | s2cid = 232299293 | url = }}</ref><ref name="pmid32991496">{{cite journal | vauthors = Kang JY, Kim HJ, Wojno TH, Yeung AM, Mendoza PR, Grossniklaus HE | title = Atypical Lipomatous Tumor/Well-Differentiated Liposarcoma of the Orbit: Three Cases and Review of the Literature | journal = Ophthalmic Plastic and Reconstructive Surgery | volume = 37 | issue = 3S | pages = S134–S140 | date = 2021 | pmid = 32991496 | doi = 10.1097/IOP.0000000000001804 | s2cid = 222143763 | url = }}</ref> This terminology has prognostic implications: less than 7% of ALT tumors convert to dedifferentiated liposarcomas within a median time of 7 years while 17% of WDL tumors convert to this more malignant liposarcoma within a median time of 8 years.<ref name="pmid33659920"/> ALT and WDL (hereafter termed ALT/WDL) tumors typically present in middle-aged and older individuals as slowly enlarging masses that tend to be larger and at a more advanced stage when located in deep tissues.<ref name="pmid30852045"/><ref name="pmid18000364"/> These tumors usually are not painful and if located superficially, readily apparent; they can also cause extensive [[edema]] (i.e. swelling due to the local accumulation of fluid) in involved areas such as the thigh (see adjacent figure) due to their invasion into the blood and/or [[lymphatic vessel]]s draining the tumor's site. Deep-seated ALT/WDL tumors may be asymptomatic but, depending on their location, produce serious signs and/or symptoms of disfunction in any one of the various organs which they infiltrate. These organs include those close to or in the retroperitoneum (e.g. intestines, kidney, and the kidney's [[ureters]]); the paratesticular region; the mediastinum (e.g. [[trachea]] and lung's [[Bronchus|major bronchi]]); and the head (e.g. the retrobulbar space behind the globe of the eye).<ref name="pmid33734108"/><ref name="pmid32991496"/>

====Pathology====
[[File:Histopathology of an atypical lipomatous tumor or well-differentiated liposarcoma, lipoma-like subtype.jpg|thumb|ALT/WDL, adipocytic/lipoma-like. At low magnification, the tumor mostly contains adipocytes that appear benign and mature, but high magnification of one fibrous band shows abnormal spindle-shaped cells with enlarged, [[heterochromatic]] nuclei.]]

Histopathologically, ALT/WDL tumors are divided into adipocytic/lipoma-like, sclerosing, and inflammatory variants with adipocyte/lipoma-like being the most common. Adipocytic/lipoma-like ALT/WDL tumors consist of lobules of mature fat cells variably intersected with irregular fibrous [[Septum|septa]] (see the adjacent [[H&E stain]]ed [[photomicrograph]]). Sclerosing ALT/WDL tumors, the second most common variant, develop primarily in the retroperitoneal and paratesticular areas; it consists of scattered, atypical [[stromal cell]]s within a collagenous (i.e. [[collagen]]-containing) [[Stroma (tissue)|stromal tissue]] background. Rare [[vacuole]]-containing [[lipoblast]]s  populate this tissue. Inflammatory ALT/WDL tumors are the rarest variant. they occur most frequently in the retroperitoneum and consists of [[Inflammation#Chronic inflammation|chronic inflammatory]] cells, e.g. [[lymphocytes]] and [[plasma cells]] plus occasional [[Lymph node|lymph node-like follicles]] interspersed throughout a tissue background containing [[fat cells]].<ref name="pmid32991496"/>

====Genetics====
The neoplastic cells in ALT/WDL tumors contain one or more extra ring-shaped [[small supernumerary marker chromosome]] (sSMC) or an abnormal giant marker chromosome (i.e. a formerly normal chromosome that is made abnormal by having a duplication of parts of its own or one or more other chromosome's genetic material). These abnormal chromosomes contain extra copies of [[chromosome 12]]'s long arm  (also termed the [[Locus (genetics)#Nomenclature|q arm]]) at [[Karyotype#Chromosome banding|bands]] 13 through 15. This stretch of chromosome 12 includes the ''[[MDM2]]'' [[oncogene#Proto-oncogene|proto-oncogene]] (a potentially tumor-causing gene when [[Glossary of genetics#overexpression|overexpressed]]) located at band 15<ref>{{Cite web|url=https://www.ncbi.nlm.nih.gov/gene/4193|title = MDM2 MDM2 proto-oncogene &#91;Homo sapiens (Human)&#93; - Gene - NCBI}}</ref> and ''[[CDK4]]'' (a gene that when overexpressed promotes the development of various tumors) located at band 14.1.<ref>{{Cite web|url=https://www.ncbi.nlm.nih.gov/gene/1019|title = CDK4 cyclin dependent kinase 4 &#91;Homo sapiens (Human)&#93; - Gene - NCBI}}</ref><ref name="pmid27073568">{{cite journal | vauthors = Nishio J, Iwasaki H, Shibata T, Nabeshima K, Naito M | title = Duplication of chromosome segment 12q13-15 in a lipomatous tumor with minimal nuclear atypia: A case report | journal = Oncology Letters | volume = 11 | issue = 4 | pages = 2875–2878 | date = April 2016 | pmid = 27073568 | pmc = 4812505 | doi = 10.3892/ol.2016.4305 | url = }}</ref> The [[Gene amplification|amplification]] (i.e. increased copies of a gene without a proportional increase in other genes) of these two genes is a highly sensitive and specific indicator that a liposarcoma is either an ALT/WDL or a dedifferentiated liposarcoma rather than any other liposarcoma or [[lipoma#types|lipoma]] form.<ref name="pmid27073568"/> In addition to the ''MDM2'' and ''CDK4'' genes, this band 13–15 chromosome area also contains the ''[[TSPAN31]]'' and ''[[HMGA2]]'' genes which, when overexpressed, are associated with various tumors and/or cancers. One or more of these overexpressed genes, it has been suggested, promote and/or contribute to the development and/or progression of ALT/WDL tumors.<ref name="pmid30852045"/>

====Diagnosis====
The diagnosis of ALT/WDL tumors is made based on the features of their clinical presentations, histopathology, and genetic findings. In particular, detection in the ALT/WDL tumor cells of an overexpressed ''MDM2'' or ''CDK4'' gene or the presence of either the specific ALT/WDL-associated sSMC or giant marker chromosome (as defined by [[DNA sequencing#High-throughput sequencing (HTS)|next generation DNA sequencing]], [[comparative genomic hybridization]],<ref name="pmid32399795">{{cite journal | vauthors = Slimani W, Jelloul A, Al-Rikabi A, Sallem A, Hasni Y, Chachia S, Ernez A, Chaieb A, Bibi M, Liehr T, Saad A, Mougou-Zerelli S | title = Small supernumerary marker chromosomes (sSMC) and male infertility: characterization of five new cases, review of the literature, and perspectives | journal = Journal of Assisted Reproduction and Genetics | volume = 37 | issue = 7 | pages = 1729–1736 | date = July 2020 | pmid = 32399795 | doi = 10.1007/s10815-020-01811-9 | url = | pmc = 7376793 }}</ref> and/or [[Cytogenetics#Advent of banding techniques|highly specialized cytogenetic G banding analyses]]<ref name="pmid32536972">{{cite journal | vauthors = Lu Y, Liang Y, Ning S, Deng G, Xie Y, Song J, Zuo N, Feng C, Qin Y | title = Rare partial trisomy and tetrasomy of 15q11-q13 associated with developmental delay and autism spectrum disorder | journal = Molecular Cytogenetics | volume = 13 | issue = | pages = 21 | date = 2020 | pmid = 32536972 | pmc = 7288499 | doi = 10.1186/s13039-020-00489-z | url =  | doi-access = free }}</ref>) strongly supports the diagnosis of ALT/WDL or dedifferentiated liposarcoma. The clinical presentation and histopathology differences between the latter two liposarcoma forms usually help distinguish between them.<ref name="pmid30852045"/>

====Treatment and prognosis====
ALT/WDL tumors are treated by radical surgical resection to remove all tumor neoplastic tissues. However, these tumors recur locally in 30–50% of cases. Recurrences occur most often in tumors located in less accessible sites such those in the retroperitoneum, mediastinum, and spermatic cord. These less surgically assessible tumors tend to recur repeatedly and ultimately may cause death due to their injurious effects on vital organs. While ALT/WDL tumors have very little potential to [[metastasize]], about 10% will convert to an overtly malignant and potentially metastasizing liposarcoma form, dedifferentiated liposarcoma.  The median time for this [[malignant transformation]] is about 7–9 years.<ref name="pmid30852045"/> In addition, a surgically removed ALT/WDL may recur after a variable interval as a dedifferentiated liposarcoma.<ref name="pmid33659920"/> A large [[randomized controlled trial]] comparing [[radiotherapy]] followed by surgery to surgery alone in ALT/WDL tumors found little difference between the two regimens. Smaller studies employing selective inhibitors of the protein products of the ''CDK4'' or ''MDM2'' genes implicated in ALT/WDL have shown at best only modest effects. Further studies using these or completely novel treatment regimens are under investigation.<ref name="pmid30852045"/> A review study in 2012 reported the 5 and 10 year survival rates of individuals with ALT/WDL to be 100% and 87%, respectively.<ref name="liposarcoma">{{cite web | vauthors = Gebhardt M, Buecker PJ|year=2004|title=Liposarcoma |work=ESUN |url= http://sarcomahelp.org/liposarcoma.html}}</ref>

=====Novel therapies=====
The novel therapies of ALT/WDL are the same as those listed in the Novel therapies section of Dedifferentiated liposarcoma.{{citation needed|date=September 2021}}

===Dedifferentiated liposarcoma===
Dedifferentiated liposarcomas are malignant tumors which in ~10% of cases develop in an existing atypical lipomatous tumor/well-differentiated liposarcoma (ALT/WDL) tumor or at the site were an ALT/WPL tumor was surgically removed. Individuals with a [[wikt:de novo|''de novo'']]  diagnosis of this tumor may have had an ALT/WDL that progressed to a dedifferentiated liposarcoma but went undetected because it developed asymptomatically  in a highly sequestered site such as the retroperitoneum or abdominal cavity. Many of the dedifferentiated liposarcoma tumors' clinical and genetic features are similar to those found in ALT/WDL tumors.<ref name="pmid30852045"/>

====Presentation====
Dedifferentiated lipoosarcomas (DDL) occur most frequently in middle-aged and older adults with a peak incidence in their sixth to eighth decades.<ref name="pmid30852045"/> Rarely, these tumors have developed in children and adolescents.<ref name="pmid34191084"/> DDL tumors most commonly occur in the retroperitoneal space but, similar to ALT/WDL, may occur in the extremities, paratesticular area, mediastinum, head, or neck.<ref name="pmid30852045"/> Less than 1% of all DDLs develop in superficial soft tissues<ref name="pmid30852045"/> or the eye socket.<ref name="pmid32339743">{{cite journal | vauthors = Yamazaki D, Ogihara N, Horiuchi T | title = Primary Orbital Dedifferentiated Liposarcoma | journal = World Neurosurgery | volume = 139 | issue = | pages = 604–607 | date = July 2020 | pmid = 32339743 | doi = 10.1016/j.wneu.2020.04.069 | s2cid = 216594976 | url = }}</ref> At presentation, DDL tumors typically are painless, large, may have been slowly and progressively enlarging for years,<ref name="pmid30852045"/> and on routine [[X-rays]] contain areas of calcium deposition (exemplified by Fig. 1 in the Histopathology of liposarcomas section).<ref name="pmid29076540">{{cite journal | vauthors = Yamashita K, Kohashi K, Yamada Y, Ishii T, Nishida Y, Urakawa H, Ito I, Takahashi M, Inoue T, Ito M, Ohara Y, Oda Y, Toyokuni S | title = Osteogenic differentiation in dedifferentiated liposarcoma: a study of 36 cases in comparison to the cases without ossification | journal = Histopathology | volume = 72 | issue = 5 | pages = 729–738 | date = April 2018 | pmid = 29076540 | doi = 10.1111/his.13421 | s2cid = 3829557 | url = }}</ref><ref name="pmid32190631">{{cite journal | vauthors = Chen HG, Zhang K, Wu WB, Wu YH, Zhang J, Gu LJ, Li XJ | title = Combining surgery with 125I brachytherapy for recurrent mediastinal dedifferentiated liposarcoma: A case report and review of literature | journal = World Journal of Clinical Cases | volume = 8 | issue = 5 | pages = 939–945 | date = March 2020 | pmid = 32190631 | pmc = 7062618 | doi = 10.12998/wjcc.v8.i5.939 | url =  | doi-access = free }}</ref> Less commonly, affected individuals have signs and/or symptoms due to their tumor's impingement on an organ (e.g. abdominal pain caused by blockage of the intestines or [[urinary tract obstruction]] caused by blockage of the [[urethra]]). Very rarely, individuals with DDL present with one or more signs or symptoms of [[Inflammation#Chronic inflammation|chronic inflammation]] (see [[B symptoms]]) and/or one of the [[paraneoplastic syndrome#Endocrine|endrocrine]], [[paraneoplastic syndrome#Neurological|neurological]], [[paraneoplastic syndrome#Mucocutaneous|mucocutaneous]], [[paraneoplastic syndrome#hematological|hematological]], or other tissue-related [[paraneoplastic syndrome]]s. The signs and symptoms of chronic inflammation and the various paraneoplastic syndromes are caused by the tumors' secretion of [[cytokines]], [[hormones]], [[prostaglandin]]s, and/or other systemically acting agents; they completely disappear after the DDL is successfully treated.<ref name="pmid30852045"/>

====Pathology====
The [[histopathological]] appearance of DDL tumors (see Fig. 2 in the below Histopathology of liposarcomas section) varies widely but most frequently exhibits features of [[undifferentiated pleomorphic sarcoma]]s (which are tumors densely populated with variably sized and shaped cells containing variability sized and shaped [[Cell nucleus|nuclei]]) or [[spindle cell sarcoma]]s (which are tumors consisting of spindle-shaped cells in a [[connective tissue]] background). Different parts of DDL tumors often show variations in the appearances of their background connective tissues: these tissues may be myxoid (i.e. consisting of a clear, [[mucus]]-like substance which when stained using a standard [[H&E stain]] method appears more blue or purple than the red color of normal tissues) or myxocollagenous (i.e. high [[collagen]] fiber content in a myxoid background), and, in ~5% of cases, have areas of [[osteoid]] (see Fig. 1 in the below Histopathology of liposarcomas section) or [[Cartilage|cartilaginous]] [[Matrix (biology)|material]]. The tumors also show large variations in their cell contents. For example, up to 10% of DDL tumors have areas with ALT/WDL histopathology <ref name="pmid30852045"/> and rare cases of DDL have areas containing meningothelial-like whorls of flat cells.<ref name="pmid23634770">{{cite journal | vauthors = Li J, Fang L, Killer HE, Flammer J, Meyer P, Neutzner A | title = Meningothelial cells as part of the central nervous system host defence | journal = Biology of the Cell | volume = 105 | issue = 7 | pages = 304–15 | date = July 2013 | pmid = 23634770 | doi = 10.1111/boc.201300013 | s2cid = 207094296 | url = }}</ref><ref name="pmid32419561">{{cite journal | vauthors = Usman Tariq M, Kayani N, Moatter T, Din NU | title = Dedifferentiated Liposarcoma With Meningothelial-Like Whorls: Five Additional Cases and Review of the Literature | journal = International Journal of Surgical Pathology | volume = 28 | issue = 7 | pages = 749–758 | date = October 2020 | pmid = 32419561 | doi = 10.1177/1066896920921950 | s2cid = 218680437 | url = }}</ref>

====Genetics====
The neoplastic cells in both DDL and ALT/WDL carry similar [[small supernumerary marker chromosome]]s (sSMCs) and/or giant marker chromosomes that contain extra parts of chromosome 12's q arm at [[G banding|bands]] 13 through 15. This chromosomal area includes two genes associated with tumor development, the ''[[MDM2]]''<ref>{{Cite web|url=https://www.ncbi.nlm.nih.gov/gene/4193|title = MDM2 MDM2 proto-oncogene &#91;Homo sapiens (Human)&#93; – Gene – NCBI}}</ref> and ''[[CDK4]]'' genes.<ref>{{Cite web|url=https://www.ncbi.nlm.nih.gov/gene/1019|title = CDK4 cyclin dependent kinase 4 &#91;Homo sapiens (Human)&#93; – Gene – NCBI}}</ref><ref name="pmid27073568"/> The presence of extra copies of these two genes and/or their overproduced protein products is a highly sensitive and specific indicator that a lipomatous tumor is an ALT/WDL or DDL rather than some other type of lipomatous tumor.<ref name="pmid33734108"/><ref name="pmid27073568"/> Overexpression of the ''MDM2'' and ''CDK'' genes, and/or other genetic material in the sSMCs or giant marker chromosomes are suspected of promoting the development and/or progression of DDL as well as ALT/WDL tumors.<ref name="pmid29279323">{{cite journal | vauthors = Macchia G, Severgnini M, Purgato S, Tolomeo D, Casciaro H, Cifola I, L'Abbate A, Loverro A, Palumbo O, Carella M, Bianchini L, Perini G, De Bellis G, Mertens F, Rocchi M, Storlazzi CT | title = The Hidden Genomic and Transcriptomic Plasticity of Giant Marker Chromosomes in Cancer | journal = Genetics | volume = 208 | issue = 3 | pages = 951–961 | date = March 2018 | pmid = 29279323 | pmc = 5844343 | doi = 10.1534/genetics.117.300552 | url = }}</ref> Other genes in the  sMMC and giant marker chromosome that are also overexpressed in ALT/WDL and DDL neoplastic cells include ''[[HMGA2]], [[CPM (gene)|CPM]], YEATS4,''<ref>{{Cite web|url=https://www.ncbi.nlm.nih.gov/gene/8089|title = YEATS4 YEATS domain containing 4 &#91;Homo sapiens (Human)&#93; – Gene – NCBI}}</ref> and ''[[DDIT3]]''. Compared to ALT/WDL neoplastic cells, however, DDL neoplastic cells: '''1)''' express higher levels of the genes in the two abnormal chromosomes; this may contribute to the progression of ALT/WDL to DDL; and '''2)''' higher levels of gene products on the long arm of chromosome 1 at band 32, the long arm of chromosome 6 at band 33, and, in ~25% of cases, the short arm of chromosome 1 at band 32.2 which contains the ''JUN'' gene (this gene is overexpressed in DDL but not ALT/WDL). Since the ''JUN'' gene's product, [[c-jun]], inhibits cell death and promotes cell proliferation, its overproduction may contribute to the progression of ALT/WDL to DDL and/or the malignancy of DDL neoplastic cells.<ref name="pmid30852045"/> [[Gene expression profiling]] (i.e. measurement of the expression of the products of thousands of genes made by cells, tissues, or tumors) have revealed that adipocyte [[Cellular differentiation|cell differentiation]] and [[metabolic pathway]]s in ALT/WDL are [[Downregulation and upregulation|upregulated]] while [[cell proliferation]] and [[DNA repair|DNA damage response]] pathways are upregulated in DDL.<ref name="pmid33659920"/>

====Diagnosis====
The histopathological of DDL is often insufficiently clear to make a firm diagnosis. However, the diagnosis of DDL is supported in individuals: whose tumors contain ALT/WDL admixed with DDL histological  components; with histories of having a prior ALT/WDL;<ref name="pmid30852045"/> or who present with a retroperitoneal liposarcoma (DDL constitutes ~57% of all retroperitoneal liposarcomas). DDL tumors only rarely (<1% of cases) present as superficial skin tumors;<ref name="pmid30852045"/> are almost 5 times less likely than ALT/WDL to occur in the eye socket;<ref name="pmid32991496"/><ref name="pmid32339743"/> and are extremely rare in children.<ref name="pmid34191084"/> Detection of tumor cell MDM2 amplification is the diagnostic gold standard in distinguishing WDL from lipomas, dysplastic lipomas, atypical spindle cell sarcomas, pleomorphic lipomas, and solitary fibrous tumors.<ref name="pmid30852045"/> Alternately, detection in the tumor cells of an overexpressed ''CDK4'' gene or the presence of either the specific ALT/WDL-associated sSMCs or giant marker chromosome strongly support the diagnosis of DDL or ALT/WDL.<ref name="pmid32399795"/><ref name="pmid32536972"/> The clinical presentation, histopathology, and gene differences (e.g. tumor cell overexpression of the ''cJUN'' gene strongly favors the diagnosis of DDL over ATL/WDL) between the latter two liposarcoma forms usually help distinguish between them.<ref name="pmid30852045"/>

====Treatment and Prognosis====
Complete surgical resection is usually the recommended first-line treatment for localized DDL tumors.<ref name="pmid33659920"/> However, emerging studies suggest that patients with DDL tumors that are restricted to an extremity or the [[trunk (anatomy)|trunk]] and have a predicted 10-year tumor-related overall survival of 51% or less have improved outcomes when [[chemotherapy]] (e.g. [[doxorubicin]] plus [[ifosfamide]]) is added to their surgical regimens.<ref name="pmid30690293">{{cite journal | vauthors = Pasquali S, Pizzamiglio S, Touati N, Litiere S, Marreaud S, Kasper B, Gelderblom H, Stacchiotti S, Judson I, Dei Tos AP, Verderio P, Casali PG, Woll PJ, Gronchi A | title = The impact of chemotherapy on survival of patients with extremity and trunk wall soft tissue sarcoma: revisiting the results of the EORTC-STBSG 62931 randomised trial | journal = European Journal of Cancer | volume = 109 | issue = | pages = 51–60 | date = March 2019 | pmid = 30690293 | doi = 10.1016/j.ejca.2018.12.009 | s2cid = 59341549 | url = }}</ref> For these localized forms of DDL, perioperative [[radiotherapy]] following [[National Comprehensive Cancer Network]] guidelines may also be considered.<ref name="pmid30852045"/>

Retroperitoneal DDL is the most common, surgically unaccessible and serious form of DDL: it has a recurrence rate of 66% and a five-year overall survival rate of 54%.<ref name="pmid34150840">{{cite journal | vauthors = Chen J, Hang Y, Gao Q, Huang X | title = Surgical Diagnosis and Treatment of Primary Retroperitoneal Liposarcoma | journal = Frontiers in Surgery | volume = 8 | issue = | pages = 672669 | date = 2021 | pmid = 34150840 | pmc = 8211986 | doi = 10.3389/fsurg.2021.672669 | url = | doi-access = free }}</ref> The primary treatment option for retroperitoneal DDL is surgical resection. A [[Clinical trial#phases|phase III clinical trial]]  found little difference in the results of [[radiation therapy]] followed by surgical resection compared to surgical resection alone in the treatment of retroperitoneal DDL.<ref name="pmid33659920"/> In other phase III clinical trials, DDL patients with inaccessible retroperitoneal and/or metastatic tumors were treated with front-line chemotherapy comparing doxorubicin to doxorubicin plus ifosfamide or doxorubicin to [[gemcitabine]] plus [[docetaxel]]. Other studies have likewise examined the value of various chemotherapy regimens. These studies often found little difference in the overall survival times in their comparisons but did show some improvements in [[progression-free survival]] and other clinical parameters. Based on these studies, a recommended first-line therapy for retroperitoneal and other surgically inassessible or metastatic DDL tumors is treatment with an anthracycline-based chemotherapy regimen or, in tumor-resistant or relapsed cases, [[eribulin]] chemotherapy. A review conducted in 2020 reported median survival times for low histopathological grade and high histopathological grade DDL to be 113 months and 48 months, respectively.<ref name="pmid32774015">{{cite journal | vauthors = Amer KM, Congiusta DV, Thomson JE, Elsamna S, Chaudhry I, Bozzo A, Amer R, Siracuse B, Ghert M, Beebe KS | title = Epidemiology and survival of liposarcoma and its subtypes: A dual database analysis | journal = Journal of Clinical Orthopaedics and Trauma | volume = 11 | issue = Suppl 4 | pages = S479–S484 | date = July 2020 | pmid = 32774015 | pmc = 7394804 | doi = 10.1016/j.jcot.2020.04.013 | url = }}</ref> Further studies are needed to provide evidence on the efficacies of radiotherapy, chemotherapy, and novel therapies in all the varieties of DDL.<ref name="pmid34213610">{{cite journal | vauthors = Lam MB, Baldini EH, Reijers SJ, Haas RL, DeLaney TF | title = Role of Radiation Therapy for Newly Diagnosed Retroperitoneal Sarcoma | journal = Current Treatment Options in Oncology | volume = 22 | issue = 9 | pages = 75 | date = July 2021 | pmid = 34213610 | doi = 10.1007/s11864-021-00877-6 | s2cid = 235701424 | url = | hdl = 1887/3281923 | hdl-access = free }}</ref>

====Novel therapies====
Several novel therapy regimens for DDL and the more aggressive or otherwise problematic cases of ALT/WDL are currently undergoing [[clinical trial]]s. A [[Phases of clinical research#Phase II|phase II]] clinical study investigating [[abemaciclib]] is underway in patients with pretreated or untreated DDL. Preliminary analysis showed that this inhibitor of the ''CDK4'' and ''CDK6'' genes' product [[Serine/threonine-specific protein kinase]] enzymes produced a prolonged median progression-free survival time of 30.4 weeks.<ref name="pmid33659920"/> A [[Phases of clinical research#Phase III|phase III]] multicenter, randomized, double-blind, [[placebo]]-controlled clinical study of abemaciclib is in its active phase and will soon (as stated in July, 2021) begin recruiting 108 individuals with advanced, recurrent, and/or metastatic DDL. The study is sponsored by the Sarcoma Alliance for Research through Collaboration<ref>{{Cite web|url=https://sarcomaalliance.org/event/sarcoma-alliance-for-research-through-collaboration-2/|title = Sarcoma Alliance for Research through Collaboration}}</ref> in collaboration with [[Eli Lilly and Company]].<ref name="clinicaltrials.gov">{{Cite web|url=https://clinicaltrials.gov/ct2/show/NCT04967521?term=abemaciclib&cond=Dedifferentiated+Liposarcoma&draw=2&rank=1|title = SARC041: Phase 3 Randomized Double-Blind Study of Abemaciclib Versus Placebo in Patients with Advanced Dedifferentiated Liposarcoma|date = 23 July 2021}}</ref> [[Ribociclib]], also a ''CDK4'' and ''CDK6'' gene inhibitor, in combination with a [[mTOR]] inhibitor, [[everolimus]] is in a phase II clinical trial in individuals with advanced DDL or [[leiomyosarcoma]].<ref name="clinicaltrials.gov"/> A phase III registration study (i.e. a large confirmatory study meant to establish an acceptable benefit/safety profile in order to gain regulatory approval for a precisely defined indication) is evaluating the safety and efficacy of [[milademetan]] compared to trabectedin in patients with unresectable (i.e., resection is deemed to cause unacceptable morbidity or mortality) or metastatic DDL that has progressed on 1 or more prior systemic therapies, including at least 1 anthracycline-based therapy. The sponsor, Rain Therapeutics Inc, is currently recruiting 160 individuals for the trial.<ref>{{Cite web|url=https://clinicaltrials.gov/ct2/show/NCT04979442?cond=Dedifferentiated+Liposarcoma&draw=2&rank=1|title = A Randomized Multicenter Phase 3 Study of Milademetan Versus Trabectedin in Patients with Dedifferentiated Liposarcoma|date = 16 July 2021}}</ref> Another phase III clinical trial is investigating the [[MDM2]] inhibitor milademetan<ref>{{Cite web|url=https://pubchem.ncbi.nlm.nih.gov/compound/Milademetan?form=MY01SV&OCID=MY01SV|title = Milademetan}}</ref> versus [[trabectedin]], a blocker of the oncogenic [[transcription factor]] [[FUS-CHOP]], in [[MDM2]]-overexpressing ALT/WDL and DDL.<ref>{{Cite web|url=https://clinicaltrials.gov/ct2/show/NCT04979442?term=mdm2&cond=Dedifferentiated+Liposarcoma&draw=2&rank=1|title=A Randomized Multicenter Phase 3 Study of Milademetan Versus Trabectedin in Patients with Dedifferentiated Liposarcoma|date=16 July 2021}}</ref> Milademetan has shown manageable toxicity and some activity resulting in stable disease and/or a few partial responses in DDL.<ref name="pmid33659920"/>

===Myxoid liposarcoma===
{{Main|Myxoid liposarcoma}}
====Presentation====
Myxoid liposarcoma (MLS), which includes a type of liposarcoma termed round cell liposarcoma,<ref name="StatPearls">{{Cite book|chapter-url=https://www.ncbi.nlm.nih.gov/books/NBK538265/|title=StatPearls|chapter=Liposarcoma|year=2021|publisher=StatPearls|pmid=30855853 | vauthors = Zafar R, Wheeler Y }}</ref> represents ~30% of all liposarcomas. It has a peak incidence in individuals' fourth and fifth decades with a male predominance in most studies. While uncommon in children and adolescents, MLS is the most common liposarcoma form diagnosed in these age groups. MLS typically presents as a large (1 to 39&nbsp;cm; average 12&nbsp;cm), mobile, well-circumscribed, painless mass that developed from 1 week to 15 years prior to diagnosis. MLS tumors are located in deep-seated soft tissues of the  thighs (65–80% of cases), lower legs (10–15% of cases), retroperitoneum (8% of cases), and arms (5% of cases). In about one-third of cases, these tumors metastasize to other soft tissue sites (e.g. retroperitoneum, thorax, or other extremity), skeletal bone, and/or lung. Individuals may present with these metastasis, particularly those in bone; it has been recommended that patients should be tested at presentation for bone metastasis by [[medical imaging]], including [[X-ray]]s, [[CT scan]]s, and/or [[magnetic resonance imaging]].<ref name="pmid31813645">{{cite journal | vauthors = Mujtaba B, Wang F, Taher A, Aslam R, Madewell JE, Nassar S | title = Myxoid Liposarcoma With Skeletal Metastases: Pathophysiology and Imaging Characteristics | journal = Current Problems in Diagnostic Radiology | volume = 50 | issue = 1 | pages = 66–73 | date = 2021 | pmid = 31813645 | doi = 10.1067/j.cpradiol.2019.10.008 | s2cid = 208954696 | url = }}</ref>

====Pathology====
Histopathologic analyses of MLS (see Figs. 3 and 4 in the below Histopathology of liposarcomas section) reveals cells scattered throughout a myxoid matrix (i.e. a connective tissue background that appears more blue or purple than the red color of normal connective tissue when these tissues are properly prepared, [[H&E stain]]ed, and viewed microscopically). These cells are [[lipoblast]]s, some of which are [[Signet ring cell|signet ring-shaped]] (a shape suggesting that the cell may be neoplastic), oval-shaped, or round-shaped.<ref name="pmid31813645"/> MLS tumors may be hypercellular and contain solid sheets of round cells that comprise at least 5% of all cells or low cellularity populated with cells that have bland nuclei and <5% round cells in a background of curving capillaries resembling a chicken-wire pattern. Tumors that contain at least 5% round cells are classified as high-grade while those with <5% round cells are classified as low-grade.<ref name="StatPearls"/> High-grade MLS tumors typically take a more aggressive clinical course than low-grade MLS tumors.<ref name="pmid31813645"/>

====Genetics====
MLS tumor cells are virtually defined by their expression of a ''FUS-DDIT3'' [[fusion gene]] (also termed a [[chimeric gene]]) which occurs in >95% of cases or a ''EWSR1-DDIT3'' fusion gene which occurs in the remaining <5% of cases. The ''FUS-DDIT3'' fusion gene forms as a result of a [[chromosomal translocation|translocation]] (termed t(12:16)(q13:p11)) between the site of the ''[[DDIT3]]'' gene <ref>{{Cite web|url=https://www.ncbi.nlm.nih.gov/gene/1649|title = DDIT3 DNA damage inducible transcript 3 &#91;Homo sapiens (Human)&#93; – Gene – NCBI}}</ref> at band 12 of chromosome 12's q arm and the site of the [[FUS (gene)|FUS]] gene<ref>{{Cite web|url=https://www.ncbi.nlm.nih.gov/gene/2521|title = FUS FUS RNA binding protein &#91;Homo sapiens (Human)&#93; – Gene – NCBI}}</ref> at band 11 on chromosome 16's short arm (also termed the [[Locus (genetics)#Nomenclature|p arm]]). The [[fusion protein]] (also termed chimeric protein) product of this chimeric [[oncogene]] gene, FUS-DDIT3, is known to arrest fat cell maturation and promote neoplasia. The ''EWSR1-DDIT3'' fusion gene (termed  t(12;22)(q13;q12)) results from a translocation of the ''[[EWSR1]]'' gene<ref>{{Cite web|url=https://www.ncbi.nlm.nih.gov/gene/2130|title = EWSR1 EWS RNA binding protein 1 &#91;Homo sapiens (Human)&#93; – Gene – NCBI}}</ref> located at band 12.2 on chromosome 22's q arm with the ''DDIT2'' gene. The fusion protein product of the ''EWSR1-DDIT3'' gene, like the FUS-DDIT3 fusion protein, promotes neoplasia.<ref name="pmid33731886">{{cite journal | vauthors = Baranov E, Black MA, Fletcher CD, Charville GW, Hornick JL | title = Nuclear expression of DDIT3 distinguishes high-grade myxoid liposarcoma from other round cell sarcomas | journal = Modern Pathology | volume = 34 | issue = 7 | pages = 1367–1372 | date = July 2021 | pmid = 33731886 | doi = 10.1038/s41379-021-00782-1 | pmc = 8763641 | s2cid = 232247392 | url = }}</ref> In spite of these fusion gene relations, further studies are required to define their contribution to the development and/or maintenance of MLS tumors.<ref name="pmid33659920"/>

====Diagnosis====
Low-grade and intermediate-grade MLS tumors can be identified histologically by their classic morphology of distinctive chicken-wire vasculature scattered throughout a myxoid stroma. However, high-grade MLS tumors can be difficult to distinguish from other round cell neoplasms, particularly high grade MLS tumors that consist of diffuse cell and/or pure round cell morphology to such an extent as to obscure this classic vascular-myxoid pattern. Detection of a ''DDIT3'' gene rearrangements with the ''FUS'' or ''EWSR1'' gene by [[in situ hybridization]] or [[immunohistochemistry]] or the [[RNA]] fusion transcripts of these genes by [[real-time polymerase chain reaction]]s confirms the diagnosis of high-grade as well as ambiguous cases of low-grade or intermediate-grade MLS tumors.<ref name="pmid33731886"/>

====Treatment and prognosis====
MLS has typically been treated by surgical resection but may require more radical interventions, e.g. limb amputation may be needed when a limb's [[neurovascular bundle]] is compromised. The post-surgical risk of recurrence within 3 years after surgery has been reported to be ~15% when not all tumor is removed and ~10% when tumor removal is complete.<ref name="pmid31813645"/> The addition of radiotherapy to surgical resection has improved the local control of MLS tumors and has been recommended to treat unresectable and recurrent MLS.<ref name="pmid30850231">{{cite journal | vauthors = Putra J, Al-Ibraheemi A | title = Adipocytic tumors in Children: A contemporary review | journal = Seminars in Diagnostic Pathology | volume = 36 | issue = 2 | pages = 95–104 | date = March 2019 | pmid = 30850231 | doi = 10.1053/j.semdp.2019.02.004 | s2cid = 73513220 | url = }}</ref> However, further studies are needed to determine the value of radiotherapy in treating the various varieties of MLS.<ref name="pmid31813645"/> Chemotherapy regimens using [[ifosfamide]], an [[anthracycline|anthracycline such as daunorubicin]], [[dacarbazine]], and/or [[trabectedin]] have been found useful: a phase III clinical trial showed progression-free survival times in MLS patients treated with trabectedin or dacarbazine to be 5.6 and 1.5 months, respectively. In 2015 the [[Food and Drug Administration]] approved trabectedin for use in unresectable and metastatic liposarcomas.{{citation needed|date=September 2021}}

Overall, the 10-year survival rate of MLS individuals has been 77%, a survival rate appreciably longer than other liposarcoma forms. Compared to low-risk MLS, high-risk MLS (risk defined by tumor round cell content and/or other unfavorable prognostic indicators) is associated with increased rates of metastasis and therefore a shorter survival time. Increased tumor size (≥ 10&nbsp;cm) is strongly associated with a higher grade MLS and therefore a shorter survival time. Other factors that have been associated with unfavorable outcomes in MLS include presence of tumor necrosis, age >45 years, ''[[P53]]'' gene overexpression,<ref name="pmid31813645"/> and male gender.<ref name="pmid32341520">{{cite journal | vauthors = Heijs B, Holst-Bernal S, de Graaff MA, Briaire-de Bruijn IH, Rodriguez-Girondo M, van de Sande MA, Wuhrer M, McDonnell LA, Bovée JV | title = Molecular signatures of tumor progression in myxoid liposarcoma identified by N-glycan mass spectrometry imaging | journal = Laboratory Investigation | volume = 100  |issue = 9 | pages = 1252–1261 | date = September 2020 | pmid = 32341520 | doi = 10.1038/s41374-020-0435-2 | s2cid = 216560584 | url = | doi-access = free }}</ref> The round cell form of myxoid liposarcomas also appears to have a relatively poor prognosis: in various retrospective reviews, myxoid liposarcoma was usually found to be low-grade and therefore relatively responsive to chemotherapy whereas high grade (i.e. round cell) myxoid lipsarcoma had higher rates of metastasis, behaved more aggressively, and did not respond well to chemotherapy.<ref name="pmid31813645"/> It is important to note, however, that almost all cases of myxoid liposarcomas in pediatric patients have had excellent prognoses.<ref name="pmid30850231"/>

=====Novel therapies=====
A [[PPAR-γ]] agonist (i.e. activator), efatutazone,<ref>{{Cite web|url=https://www.wikidata.org/wiki/Q27266481|title=Efatutazone dihydrochloride}}</ref> was studied in a small phase I trial on individuals with various advanced-stage malignancies. The drug produced a markedly durable response in a person with MLS suggesting that PPAR-γ agonists would be useful for treating this disease.<ref>{{Cite web|url=https://clinicaltrials.gov/ct2/show/study/NCT02249949?term=myxoid+liposarcoma&draw=2&rank=7|title = A Phase II Study of the Peroxisome Proliferator-Activated Receptor Gamma Agonist, Efatutazone in Patients with Previously Treated, Unresectable Myxoid Liposarcoma|date = 16 August 2021}}</ref> A stage II clinical trial conducted in Italy is examining the effects of a trabectedin plus [[pioglitazone]] (another PPAR-γ agonist) in individuals with stable MLS tumors. The study involves two sequential steps. The first step examines the response of patients treated for a minimum of 4 cycles with trabectedin alone. If stable disease is attained, the second step will examine the effects of further treating initially responding patients with a combination of trabectedin and pioglitazone.<ref>{{Cite web|url=https://clinicaltrials.gov/ct2/show/NCT04794127?term=myxoid+liposarcoma&draw=2&rank=4|title = A Phase II Study on Trabectedin in Combination with PPARg Agonist Pioglitazone in Patients with Round Cell Myxoid Liposarcomas or Dedifferentiated G1 and G2 Liposarcomas with Stable Disease After a Monotherapy with Trabectedin. (TRABEPIO)|date = 10 March 2021}}</ref> A stage II clinical trial is nearing completion to evaluate the efficacy of [[sirolimus]] (an inhibitor of [[MTOR]]; sirolimus is also known as rapamycin) plus [[cyclophosphamide]] (a chemotherapy drug) in metastatic or unresectable MLS.<ref>{{Cite web|url=https://clinicaltrials.gov/ct2/show/NCT02821507?cond=Myxoid+Liposarcoma&draw=2&rank=6|title = A Phase 2, Single Arm, Multi Center Trial Evaluating the Efficacy of the COmbination of Sirolimus and cYclophosphamide in Metastatic or Unresectable Myxoid Liposarcoma and chOndrosarcoma|date = 4 June 2021}}</ref> A phase II clinical trial is recruiting patients to evaluate [[sintilimab]] (a human [[IgG4]] [[monoclonal antibody]] directed against the [[programmed cell death protein 1]] located on the surface of cells) in combination with two chemotherapy drugs, [[doxorubicin]] and [[ifosfamide]], as [[Therapy#Lines of therapy|first-line treatment]] of soft tissue sarcomas including MLS.<ref>{{Cite web|url=https://clinicaltrials.gov/ct2/show/NCT04356872?recrs=ab&cond=myxoid+liposarcoma&draw=2&rank=4|title = A Single Arm, Multi Centers, Phase II Study of Sintilimab, Doxorubicin and Ifosfamide at First-line Treatment of Soft Tissue Sarcoma Including Undifferentiated Pleomorphic Sarcoma, Synovial Sarcoma, Myxoid Liposarcoma and De-differentiated Liposarcoma|date = 13 July 2020| vauthors = Luo Z }}</ref>

[[T cells]] have been [[genetically engineered]] to target the [[MAGEA4|MAGE-A4]] [[antigen]] expressed on a [[HLA-A*02]] MAGE-A4-containing peptide located on the surface of the neoplastic cells in certain types of tumors. These engineered cells (termed ADP-A2M4-T cells) attacked and killed various [[Cell culture|cultured]] human cancer cells bearing this antigen<ref name="pmid32002290">{{cite journal | vauthors = Sanderson JP, Crowley DJ, Wiedermann GE, Quinn LL, Crossland KL, Tunbridge HM, Cornforth TV, Barnes CS, Ahmed T, Howe K, Saini M, Abbott RJ, Anderson VE, Tavano B, Maroto M, Gerry AB | title = Preclinical evaluation of an affinity-enhanced MAGE-A4-specific T-cell receptor for adoptive T-cell therapy | journal = Oncoimmunology | volume = 9 | issue = 1 | pages = 1682381 | date = 2020 | pmid = 32002290 | pmc = 6959444 | doi = 10.1080/2162402X.2019.1682381 | url = }}</ref> and, in a clinical stage 1 study, shrank various solid tumor types in patients whose tumors' contained neoplastic cells expressing this antigen.<ref name="pmid32540953">{{cite journal | vauthors = | title = T Cells Targeting MAGE-A4 Shrink Tumors | journal = Cancer Discovery | volume = 10 | issue = 8 | pages = OF2 | date = August 2020 | pmid = 32540953 | doi = 10.1158/2159-8290.CD-NB2020-059 | url = | doi-access = free }}</ref> A phase II clinical study is has recruited individuals to investigate the efficacy and safety of ADP-A2M4 T cells (engineered from the recipient's own T cells) in HLA-A*02-positive patients with metastatic or inoperable, advanced-stage MSGE-4-positive MLS tumors.<ref>{{Cite web|url=https://clinicaltrials.gov/ct2/show/NCT04044768?cond=Myxoid+Liposarcoma&draw=2&rank=5|title = A Phase 2 Single Arm Open-Label Clinical Trial of ADP-A2M4 SPEAR™ T Cells in Subjects with Advanced Synovial Sarcoma or Myxoid/Round Cell Liposarcoma|date = 18 June 2021}}</ref>

===Pleomorphic liposarcoma===
====Presentation====
Pleomorphic liposarcomas (PLS), which account for 5% to 10% of all liposarcoma cases,<ref name="pmid29465602">{{cite journal | vauthors = Wang L, Luo R, Xiong Z, Xu J, Fang D | title = Pleomorphic liposarcoma: An analysis of 6 case reports and literature review | journal = Medicine | volume = 97 | issue = 8 | pages = e9986 | date = February 2018 | pmid = 29465602 | pmc = 5841962 | doi = 10.1097/MD.0000000000009986 | url = }}</ref> are fast-growing, usually large (>5&nbsp;cm), and painless but highly malignant adipocyte tumors.<ref name="pmid33802620">{{cite journal | vauthors = Libbrecht S, Van Dorpe J, Creytens D | title = The Rapidly Expanding Group of RB1-Deleted Soft Tissue Tumors: An Updated Review | journal = Diagnostics | volume = 11 | issue = 3 | date = March 2021 | page = 430 | pmid = 33802620 | pmc = 8000249 | doi = 10.3390/diagnostics11030430 | url = | doi-access = free }}</ref> They occur primarily in individuals >50 years old<ref name="pmid33802620"/> with a predominance in females.<ref name="pmid30850231"/> PLS tumors are rarely found in children.<ref name="pmid33802620"/> PLS tumors present in a leg or arm (65% of cases), retroperitoneum or abdomen (15% of cases),<ref name="pmid33659920"/> or in rare cases the trunk wall, [[spermatic cord]],<ref name="pmid33802620"/> head and neck areas,<ref name="pmid28528729">{{cite journal | vauthors = Agarwal J, Kadakia S, Agaimy A, Ogadzanov A, Khorsandi A, Chai RL | title = Pleomorphic liposarcoma of the head and neck: Presentation of two cases and literature review | journal = American Journal of Otolaryngology | volume = 38 | issue = 4 | pages = 505–507 | date = 2017 | pmid = 28528729 | doi = 10.1016/j.amjoto.2017.04.012 | url = }}</ref> chest wall, [[pelvic cavity]], [[pulmonary pleurae]], [[pericardium]], and spine.<ref name="pmid29465602"/> These tumors are usually localized in deep soft tissues with only 25% of cases presenting in subcutaneous tissues.<ref name="pmid33802620"/> Rare cases of PLS have presented in individuals with the [[Li-Fraumeni syndrome|Li-Fraumeni]] or [[Muir–Torre syndrome]]s, two [[Genetic disorder|hereditary genetic disorders]] that predispose affected persons to develop various types of cancer.<ref name="pmid30850231"/>

====Pathology====
The histopathology of PLS tumors often consists of areas resembling myxoid liposarcoma<ref name="pmid30857767">{{cite journal | vauthors = Demicco EG | title = Molecular updates in adipocytic neoplasms✰ | journal = Seminars in Diagnostic Pathology | volume = 36 | issue = 2 | pages = 85–94 | date = March 2019 | pmid = 30857767 | doi = 10.1053/j.semdp.2019.02.003 | s2cid = 75135591 | url = }}</ref> mixed with areas containing  undifferentiated cells.<ref name="pmid33802620"/> These tumors are marked hypercellular and contain at least some variably shaped [[lipoblast]]s that have pleomorphic nuclei.<ref name="pmid30857767"/> Areas of necrosis are common, giant cells, some of which are multinucleated and/or contain engulfed [[neutrophils]], are occasionally present, and [[hyaline]] droplets may be seen in some cells as well as scattered extracellularly throughout the tumor.<ref>{{Cite web|url=https://www.pathologyoutlines.com/topic/softtissueadiposepleomorphiclipo.html|title = Pleomorphic liposarcoma}}</ref> The undifferentiated component of these tumors most often consists of spindle-shaped cells, with 25% of cases showing cells with an [[epithelioid cell]] morphology. These tumors have at least some foci with a histopathology similar to high-grade [[Histiocytoma|myxofibrosarcoma type histiocytomas]],<ref name="pmid33802620"/><ref name="pmid30857767"/><ref name="pmid30018380">{{cite journal | vauthors = Ogura K, Hosoda F, Arai Y, Nakamura H, Hama N, Totoki Y, Yoshida A, Nagai M, Kato M, Arakawa E, Mukai W, Rokutan H, Kawai A, Tanaka S, Shibata T | title = Integrated genetic and epigenetic analysis of myxofibrosarcoma | journal = Nature Communications | volume = 9 | issue = 1 | pages = 2765 | date = July 2018 | pmid = 30018380 | pmc = 6050269 | doi = 10.1038/s41467-018-03891-9 | bibcode = 2018NatCo...9.2765O | url = }}</ref> a tumor formerly termed malignant myxoid fibrous histiocytoma.<ref name="pmid33363928">{{cite journal | vauthors = Rachdi I, Daoud F, Khanchel F, Arbaoui I, Somai M, Zoubeidi H, Aydi Z, Ben Dhaou B, Debbiche A, Boussema F | title = Myxofibrosarcoma of the leg: A diagnostic challenge | journal = Clinical Case Reports | volume = 8 | issue = 12 | pages = 3333–3336 | date = December 2020 | pmid = 33363928 | pmc = 7752563 | doi = 10.1002/ccr3.3414 | url = }}</ref>

====Genetics====
PLS neoplastic cells contain various gene and chromosome abnormalities: the ''[[TP53]]'' gene is [[Deletion (genetics)|deleted]] or mutated in 17–60% of cases; the ''[[Retinoblastoma protein|RB1]]'' gene is deleted in 60% of cases; and the ''[[Neurofibromin 1]]'' gene is lost by inactivating [[mutation]]s in 8% of cases or in rarer cases by a deletion around its location in band 11.2 on the long arm of chromosome 12. These cells can also show gains in the genetic material around: bands 12–15 on the short arm of chromosome 5; band 21 on the short arm of chromosome 1; and band 22 on the long arm of chromosome 7. The alterations in gene copy numbers induced by these abnormalities are similar to those seen in the [[Histiocytoma|myxofibrosarcoma type of the histiocytomas]]. The role(s) of these changes in gene copy numbers in promoting PLS has not been defined. Thus, PLS is unlike other liposarcomas in that its neoplastic cells have a complex genome without characteristic genomic alterations or identifiable genes that drive the disease. Detection of alterations in the expression of the ''TP53,  RB1'', and ''neurofibromin 1'' genes, as well as other, less commonly altered genes in PLS (e.g. ''[[PIK3CA]], [[tyrosine-protein kinase SYK]], [[PTK2B]], [[EPHA5]]'', and ''[[ERBB4]]''), may help support but do not clearly define a tumor as being PLS.<ref name="pmid33659920"/><ref name="pmid33802620"/>  Extension of the chromosome [[telomere]] ends by pathological mechanisms termed [[Alternative Lengthening of Telomeres|alternative lengthening of telomeres]] occurs in the neoplastic cells of ~80% of PLS cases but is far less common or not seen in the other four forms of liposarcoma.<ref name="pmid30857767"/>

====Diagnosis====
The diagnosis of PLS depends on its presentation, histopathology, and genetics. The histopathology of PLS often closely resembles that of myxofibrosarcoma but is distinguished from that tumor by its content of pleomorphic lipoblasts.<ref name="pmid30857767"/>

====Treatment and prognosis====
Radical surgical resection is the main treatment for PLS; it is also an important palliative intervention to relieve symptoms due to the compression of organs and tissues. Surgery may require removal of an entire compressed organ such as the kidney or colon. Regardless of this surgery, however, local recurrence rates are very high. The uses of chemotherapy and/or radiotherapy in conjunction with radical surgery have not been shown to prolong survival and are regarded as controversial interventions.<ref name="pmid29465602"/> The [[National Comprehensive Cancer Network]] recommends treatment for individuals with high-risk localized PLS by complete surgical resection, when feasible, combined with radiation therapy. Individuals with metastatic disease have been treated with chemotherapy (e.g. [[doxorubicin]] plus [[ifosfamide]] or [[eribulin]]) similar to the regimens used for dedifferentiated liposarcoma (see above section on the treatment of this liposarcoma type)<ref name="pmid33659920"/> About 20% of PLS tumors metastasize to distant sites, the most common of which are lung (82% of metastases), liver (18% of metastases), and bone or [[pancreas]] (18% of metastases). PLS survival rates at 1, 3, and 5 years are reported to be 93%, 75%, and 29%, respectively. Tumors located in the center position of the trunk, larger than 10&nbsp;cm in size, deeply seated, or containing areas of necrosis have worse prognoses.<ref name="pmid29465602"/>

===Myxoid pleomorphic liposarcoma===
Myxoid pleomorphic liposarcoma (originally termed pleomorphic myxoid liposarcoma<ref name="pmid34168281">{{cite journal | vauthors = Creytens D, Folpe AL, Koelsche C, Mentzel T, Ferdinande L, van Gorp JM, Van der Linden M, Raman L, Menten B, Fritchie K, von Deimling A, Van Dorpe J, Flucke U | title = Myxoid pleomorphic liposarcoma-a clinicopathologic, immunohistochemical, molecular genetic and epigenetic study of 12 cases, suggesting a possible relationship with conventional pleomorphic liposarcoma | journal = Modern Pathology | volume = 34| issue = 11| pages = 2043–2049| date = June 2021 | pmid = 34168281 | doi = 10.1038/s41379-021-00862-2 | s2cid = 235614580 | url = | doi-access = free }}</ref>) was first described in a large 2009 study of the liposarcomas.<ref name="pmid19194281">{{cite journal | vauthors = Alaggio R, Coffin CM, Weiss SW, Bridge JA, Issakov J, Oliveira AM, Folpe AL | title = Liposarcomas in young patients: a study of 82 cases occurring in patients younger than 22 years of age | journal = The American Journal of Surgical Pathology | volume = 33 | issue = 5 | pages = 645–658 | date = May 2009 | pmid = 19194281 | doi = 10.1097/PAS.0b013e3181963c9c | s2cid = 21863759 }}</ref> While initially regarded as a possible variant of the myxoid liposarcomas with [[Pleomorphism (cytology)|pleomorphic]] features, the [[World Health Organization]] (2020) classified it as a new and distinct form of the liposarcomas. This classification was based on findings that the myxoid pleomorphic liposarcomas, while having histopathological features that were similar to myxoid liposarcomas, had clinical and, most importantly, critical genetic and molecular features that differed from the myxoid as well as the other three liposarcoma forms.<ref name="pmid34191084"/>

====Presentation====
Myxoid pleomorphic liposarcoma (MPL) is an exceptionally rare and highly aggressive form of the liposarcomas that develops in children, adolescents,<ref name="pmid34191084"/> young adults,<ref name="pmid33659920"/> and, in a more recent study, individuals >50 years old.<ref name="pmid34168281"/> MPL tumors present as deep soft-tissue masses that are often located in the mediastinum<ref name="pmid33731886"/> and, less often, the extremities, head and neck, abdominal cavity, or trunk.<ref name="pmid33659920"/> At least two case of MPL have presented in individuals with the [[Li–Fraumeni syndrome]], an inherited [[genetic disorder]] that predisposes individuals to develop various cancers.<ref name="pmid30857767"/><ref name="pmid31559875">{{cite journal | vauthors = Zare SY, Leivo M, Fadare O | title = Recurrent Pleomorphic Myxoid Liposarcoma in a Patient With Li-Fraumeni Syndrome | journal = International Journal of Surgical Pathology | volume = 28 | issue = 2 | pages = 225–228 | date = April 2020 | pmid = 31559875 | doi = 10.1177/1066896919878804 | s2cid = 203568504 | url = }}</ref><ref name="pmid28160093">{{cite journal | vauthors = Sinclair TJ, Thorson CM, Alvarez E, Tan S, Spunt SL, Chao SD | title = Pleomorphic myxoid liposarcoma in an adolescent with Li-Fraumeni syndrome | journal = Pediatric Surgery International | volume = 33 | issue = 5 | pages = 631–635 | date = May 2017 | pmid = 28160093 | doi = 10.1007/s00383-017-4063-x | s2cid = 29704574 | url = }}</ref>

====Pathology====
On histopathologic analyses, MPL tumors consist of areas resembling conventional myxoid liposarcoma; these areas, which represent 30–50% of the total tumor areas, have an abundant myxoid matrix, a well-developed capillary vasculature, bland cells that are round and/or slightly spindle-shaped, vacuolated lipoblasts, and multinucleated cells shaped like small flowers. However, these areas also contain a scattering of  highly pleomorphic cells that show greater degrees of nuclear enlargement and irregularity than the cells seen myxoid liposarcoma tumors. Other areas of MPL tumors are more cellular and consist of rapidly growing and highly pleomorphic [[lipoblast]]s.<ref name="pmid34168281"/>

====Genetics====
The neoplastic cells in MPL do not express the ''FUS-DDIT3'' or ''EWSR1-DDIT3'' fusion genes that are expressed by the neoplastic cells in >95% or <5%, respectively, of myxoid fibrosarcoma cases.<ref name="pmid34168281"/><ref name="pmid33659920"/> Inactivation of the ''[[Retinoblastoma protein|RB1]]'' [[tumor suppressor gene]] due to its deletion or pathological suppression is found in all cases MPL. MPL neoplastic cells also commonly have other alterations in their chromosomes. They may show abnormal gains in some of the genetic material normally found on chromosomes 1, 6, 7, 8, 19, 21, and/or X and losses in the genetical material normally found on chromosomes 2, 3, 4, 5, 10, 11, 12, 13, 14, 15, 16, 17 and/or 22. The genetic material lost in band 14 on the long arm of chromosome 13 includes not only the ''[[RP1]]'' gene but also the ''[[RCBTB2]], [[DLEU1]],'' and ''[[ITM2B]]'' genes. Due to its rarity and more recent definition, the molecular characteristics and importance of these genetic abnormalities have yet to be fully defined.<ref name="pmid33802620"/> Nonetheless, studies have suggested that Losses in any one or more of the ''RB1, RCBTB2, DLEU1,'' and ''ITM2B'' genes, but particularly the ''RP1'' gene, may be involved in contributing to the development and/or progression of MPL.<ref name="pmid34168281"/>

====Diagnosis====
The diagnosis of MPL depends on its tumors clinical presentation, histopathological resemblance to myxoid liposarcoma, and, most critically, absence of the ''FUS-DDIT3'' sn ''EWSR1-DDIT3'' fusion genes in its neoplastic cells.<ref name="pmid34168281"/><ref name="pmid33659920"/>

====Treatment and prognosis====
While individuals with MPL have been treated with surgical resection to remove their tumors,<ref name="pmid31559875"/><ref name="pmid28160093"/><ref name="pmid33659920"/><ref name="pmid33738541">{{cite journal | vauthors = Peng R, Li N, Lan T, Chen H, Du T, He X, Chen M, Xie Y, Zhang Z, Zhao W, Zhang H | title = Liposarcoma in children and young adults: a clinicopathologic and molecular study of 23 cases in one of the largest institutions of China | journal = Virchows Archiv | volume = 479| issue = 3| pages = 537–549| date = March 2021 | pmid = 33738541 | doi = 10.1007/s00428-021-03076-8 | s2cid = 232273351 | url = }}</ref> a 2021 review found that there were no consensus recommendations for the standard of care for MPL with respect to radiation and chemotherapy regimens (when used either alone or combined with surgery) for treating these tumors.<ref name="pmid33659920"/>

==Histopathology of liposarcomas==
<gallery>
File:Osseous formation in a well-differentiated liposarcoma.jpg|Fig. 1 [[Micrograph]] of bone formation in a liposarcoma tumor
Image:Dedifferentiated liposarcoma - intermed mag.jpg|Fig. 2 [[Micrograph]] of a dedifferentiated liposarcoma tumor
Image:Myxoid liposarcoma (01).jpg|Fig. 3 Lower-power [[micrograph]] of myxoid liposarcoma tumor
File:Myxoid liposarcoma (06).JPG|Fig. 4 Higher-power [[micrograph]] of myxoid liposarcoma tumor
</gallery>

==Medical imaging==
[[Medical ultrasonography]] and [[magnetic resonance imaging]] (MRI) of liposarcomas are helpful and often essential in determining their extent, surgical accessibility, and relationship to any observed organ dysfunctions. Since ultrasonography is usually unable to distinguish a liposarcoma from a benign lipoma, MRI is the initial imaging of choice to provide evidence relative to making this distinction.<ref>{{cite web |url= https://radiopaedia.org/articles/lipoma|title=Lipoma| vauthors = Sharma R, Gaillard F |display-authors=etal|access-date=2018-09-27|website=Radiopaedia}}</ref>

In myxoid liposarcoma, it shows low signal intensity mass with high signal intensity foci on T1-weighted MRI images. The mass shows high signal intensity on T2-weighted images. This is because it contains predominantly [[myxoid tumor|mucoid substance]] (accounts for low signal intensity on T1) and small amount of mature fat (accounts for high signal intensity on T1).<ref name="Sung 2000">{{cite journal | vauthors = Sung MS, Kang HS, Suh JS, Lee JH, Park JM, Kim JY, Lee HG | title = Myxoid liposarcoma: appearance at MR imaging with histologic correlation | journal = Radiographics | volume = 20 | issue = 4 | pages = 1007–1019 | date = July 2000 | pmid = 10903690 | doi = 10.1148/radiographics.20.4.g00jl021007 }}</ref> The mass is well-defined, lobulated, multiloculated, or oval in shape without any infiltration into surrounding structures.<ref name="Sung 2000"/>

<gallery mode="heights=&quot;160&quot;">
Scrotal ultrasonography of liposarcoma.jpg|Fig. 5 [[Medical ultrasonography|Ultrasonography]] of a liposarcoma with high-echo areas reflected from its lipomatous matrix and low-echo areas reflected from its non-lipomatous areas.<ref name="MakTzeng2012">Content originally copied from: {{cite book | vauthors = Mak CW, Tzeng WS |title=Sonography |chapter=Sonography of the Scrotum |chapter-url=https://www.intechopen.com/books/sonography/sonography-of-the-scrotum |year=2012 |publisher=IntechOpen |doi=10.5772/27586 |isbn=978-953-307-947-9}}  under the [https://creativecommons.org/licenses/by/3.0/ CC-BY-3.0 license].</ref><!-- This is content from a predatory publisher (intechopen.com); recommend finding an alternative source for a comparable image, but I hesitate to remove the image at this time. -->
Scrotal ultrasonography of liposarcoma mimicking a lipoma.jpg|Fig. 6 [[Ultrasonography]] of a liposarcoma mimicking a lipoma. This homogeneous high-echoic mass has the same appearance as a lipoma.<ref name="MakTzeng2012"/>
HG mixoid liposarcoma, MRI, 2019, 10, 09.png|Fig. 7 [[MRI]] of myxoid liposarcoma of high grade, in the left [[axilla|axillary region]] of 40-year-old man, highlighted by its white color, in this horizontal section of the tumor.
</gallery>

==Society and culture==

===Notable cases===
* [[Chad Brown (poker player)|Chad Brown]] (1961{{ndash}}2014), a poker player, died from liposarcoma
* [[Richard Feynman]] (1918–1988), a theoretical physicist, died following surgery to address the disease.
* [[Rob Ford]] (1969{{ndash}}2016), former Toronto mayor and Toronto city councillor, died of pleomorphic liposarcoma.
* [[Hokie Gajan]] (1959{{ndash}}2016), former running back for the [[New Orleans Saints]] and radio color commentator for the team, died from liposarcoma.
* [[Charlie Davies]] (born 1986), former soccer player for the [[Philadelphia Union]] of Major League Soccer, diagnosed with liposarcoma in 2016.
* [[Mark Strand]] (1934{{ndash}}2014), former US Poet Laureate and Pulitzer Prize-winner, died from liposarcoma.

==See also==
* [[Lipoma]]
* [[Milademetan]], investigational new drug
* [[The Wendy Walk]], not-for-profit organization whose mission is to raise funds and awareness for sarcomas, including liposarcoma

==References==
{{reflist}}

{{Soft tissue tumors and sarcomas}}
{{Medical resources
|  DiseasesDB     = 31482
|  ICD10          =
|  ICD9           = 
|  ICDO           = {{ICDO|8850|3}}
|  OMIM           =
|  MedlinePlus    =
|  eMedicineSubj  = derm
|  eMedicineTopic = 856
|  MeshID         = D008080
}}
{{Authority control}}

[[Category:Dermal and subcutaneous growths]]
[[Category:Sarcoma]]
[[Category:Soft tissue disorders]]